Literature summary for 2.7.1.150 extracted from

Gan, Q.; Wang, X.; Zhang, Q.; Yin, Q.; Jian, Y.; Liu, Y.; Xuan, N.; Li, J.; Zhou, J.; Liu, K.; Jing, Y.; Wang, X.; Yang, C.
The amino acid transporter SLC-36.1 cooperates with PtdIns3P 5-kinase to control phagocytic lysosome reformation (2019), J. Cell Biol., 218, 2619-2637 .

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Protein Variants

Protein Variants	Comment	Organism
additional information	ppk-3(n2668) strong loss-of-function mutants embryos contain many vacuolar structures of different sizes, a subset of which are positive for both LAAT-1::GFP and HIS-24::mCh, indicating that they are phagolysosomes. The double mutant of slc-36.1(yq110) with ppk-3(n2668) contains enlarged autolysosomes similar to ppk-3(n2668) single mutants	Caenorhabditis elegans
S1448L	naturally occuring mutation yq24, yq24 mutants exhibit embryonic vacuoles similar to slc-36.1 mutants. Double mutants of yq24 with ced-4(n1162) show neither button-like apoptotic cell corpses nor vacuolar structures. The yq24 embryonic vacuoles are enriched for both LAAT-1::GFP and HIS-24::mCh. Mutant yq24 embryonic vacuoles are phagolysosomes arising from apoptosis	Caenorhabditis elegans

Localization

Localization	Comment	Organism	GeneOntology No.	Textmining
lysosome	-	Caenorhabditis elegans	5764	-
vacuole	lysosomal	Caenorhabditis elegans	5773	-

Metals/Ions

Metals/Ions	Comment	Organism	Structure
Mg2+	required	Caenorhabditis elegans

Natural Substrates/ Products (Substrates)

Natural Substrates	Organism	Comment (Nat. Sub.)	Natural Products	Comment (Nat. Pro.)	Rev.	Reac.
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate	Caenorhabditis elegans	-	ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate	-	?

Organism

Organism	UniProt	Comment	Textmining
Caenorhabditis elegans	G5ED98	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
embryo	-	Caenorhabditis elegans	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate	-	Caenorhabditis elegans	ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate	-	?

Synonyms

Synonyms	Comment	Organism
PIKfyve	-	Caenorhabditis elegans
PPK-3	-	Caenorhabditis elegans
PtdIns3P 5-kinase	-	Caenorhabditis elegans

Cofactor

Cofactor	Comment	Organism	Structure
ATP	-	Caenorhabditis elegans

General Information

General Information	Comment	Organism
malfunction	loss of PPK-3, the Caenorhabditis elegans homologue of the PtdIns3P 5-kinase PIKfyve, causes accumulation of phagolysosomal vacuoles that are defective in phagocytic lysosome reformation (PLR). Loss of slc-36.1 and ppk-3 causes strong defects in autophagic lysosome reformation in adult animals. Ppk-3(n2668) strong loss-of-function mutants embryos contain many vacuolar structures of different sizes, a subset of which are positive for both LAAT-1::GFP and HIS-24::mCh, indicating that they are phagolysosomes. The double mutants of slc-36.1(yq110) with ppk-3(n2668) contain enlarged autolysosomes similar to ppk-3(n2668) single mutants	Caenorhabditis elegans
metabolism	amino acid transporter SLC-36.1 and PPK-3 function in the same genetic pathway, and they directly interact with one another. The SLC-36.1-PPK-3 axis is essential for autophagic lysosome reformation (ALR)	Caenorhabditis elegans
physiological function	the phosphatidylinositol 3-phosphate (PtdIns3P) 5-kinase PIKfyve and the lysosomal calcium channel TRPML1 are required for endocytic lysosome reformation. PIKfyve generates phosphatidylinositol 3,5-bisphosphate, which activates TRPML1 to control lysosomal Ca2+ efflux. The SLC-36.1-PPK-3 axis is essential for ALR	Caenorhabditis elegans

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Release 2023.1 (January 2023)